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Neuroimaging of common neurological conditions

Introduction
In routine clinical practice, neuroimaging aims differentiating normal and
pathological nervous tissue by demonstrating nonspecific macroscopic physical
changes with a variety of radiological techniques, mostly magnetic resonance
imaging (MRI) and CT Scan. Increasingly, and with major gains in specifity, imaging
can demonstrate physiological or metabolic differences between normal and
abnormal tissue. Examples inclide :
1) Diffusion- weighted imaging (DWI) with very high specifity in acute stroke,
brain abcess, and certain tumors
2) Perfusion techniques (CT or MRI) used to triage acute stroke to allow the
delivery of hyperacute thrombolytic therapy and to accurately separate tumor
reccurence rom radiaton injury
3) Magnetic resonance spectroscopy (MRS), which shows patholognomonic
findings in brain tumors and certain dysmyelinating and degenerative
conditions
4) Function MRI (fMRI), which allows real time assessment of eloquent cortex
in the live patient.
5) Radiobuclide techniques like single photonemission SPECT and positron
emission tomography (PET), used in epilepsy, neuro- oncology, and stroke
neurology. Current recommendations for neuroimaging of common
neurologicaldisease are herein discussed according to clinical presentation.
The benefits of medical imaging are great, but one should always be warry of
the risks. Lionizing radiation from standard X-Ray imaging, including CT,
has negligible risk,, but exposure should be justifiable and limited. Lodinated
contrast is nephrotoxic in patients with poor renal function. Recently,
gadolinium contrast has been linked to nephrogenic systemic fibrosis (NSF), a
rare scleroderma-like syndrome in patients with poor renal failure. Current
recommendations are to avoid gadolinium contrast in patients in moderate or
severe renal failure; if medically necessary, patients should be informed of the
risk of developing NSF.
I.

HEADACHES

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Headaches are among the most common reasons for neurological
consultation, with 50% of adults admittedly having consulted for a severe
headache a least once in their life. Fortunately, the vast majority have a benign
origin. Pain sensitive structures in the cranial area include the scalp, the scalp
blood vessels, head and neck muscles, dural sinuses, the dura and large
cerebral arteries at the skull base, meningeal arteries, and pain sensitive
febiers of the fifth, ninth, and tenth cranial nerves. Serious conditions that
cause headaches include hemorrhage (Subarachnoid, subdural, intracerebral),
infections( meningitis, brain abcess), tumors (primary of metastatic),
hydrocephalus, and hypertensive crises. Factors that signal a serious condition
in hydrocephalus, and hypertensive crises. Factors that signal a serious
condition include :
1) Severe headache of sudden onset
2) Mental status changes, fever, focal neurologicak deficits, or seizures
3) Onset after the age of 50
1. Acute headaches. Acute headaches associated with nausea, vomiting,
nuchal rigidity, and transient alteration in mental status is extremely
suggestive of subarachnoid hemorrhage (SAH) and should prompt
immediate evaluation. CT is currently the preferred neuroimaging method
for SAH, with reported accuracy rates in the 98% to 99% range. If in diubt,
a lumbar puncture (LP) should be performed because xanthochromic CSF
is consideres the diagnostic standard for SAH
1. SAH and aneurysms. Nontraumatc SAH is caused by a ruptured
intracranial anerym in 80% to 85% of patients. About 10% of patients with
SAH, usually in the younger are group, have perimesencephalic
hemorrhage, a benign and self limiting venous hemorrhage. Catheter
angiography remains the gold standard study these patients, followed by
endovascular or surgical aneurysm obliterations. CTA is increasingly used
as a reliable replacement for cerebral angiography, including for the
surgical planning of ruptured and unruptured aneuryms by many surgeons
(FIG.32.2). Uncommon causes of SAH include cerebral tumors,
vasculitides, and moyamoya disease. Often, diagnosis and staging of these
conditions require cerebral angiography )which rules out aneurysm), and
most require further workup with MRI.
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2. intracerebral hemorrhage and other causes of acute headache.

Intracerebral hemorrhage is most commonly caused by arterial
hypertension and may putaminal, lobar, thalamic, pontine, and cerebellar.
Cerebral amyloid angiopathy (CAA) may cause lobar hemorrhage in the
non hypersetensive elderly. CT is the approved method of evaluation and
follow-up, showing a hyperdense hematoma with a surrounding hypodense
rim of edema, deforming neighboring structures. In younger,
nonhypertensive patients, a cerebral or dural arteriovenous malformation
may be the cause of hemorrhage, requiring further workup with MRI and
cerebral angiography , which may need to be repeated or delayed if there is
a large and compressive hematoma. Contrast-enhanced MRI and possibly
MR spectroscopy may be useful if a tumor is suspected.
On particularly painful and recurrent form of headache in young
subjects has been recently identified as benign thunderclap headache;
cerebral arterial spasm may be present without evidence of hemorrhage,
likely associated with generalizedabnormal vasoreactivity, similar to
preeclampsia. These patients are evaluated the same way SAH patients are.
Severe unilateral headache with cervicalgia and / or a horners syndrome
may be caused by an acute carotid or vertebral arterial dissection.
MRI/MRA especially with precontrast fat-saturated axial T1 imaging is
diagnostic, showing the true lumen as a flow void and the mural thrombus
as a bright crescent, so that there is generally no need for conventional
angiography unless intracranial extension is suspected or endovascular
treatment is expected. Migraine can cause severe acute headaches, usually
periorbital, hemifacial, and frontal. The diagnosis is clinical, and no more
than CT may be required in severe cases, as for cluster headaches. Sinusitis
is also diagnosed clinically; coronal CT shows soft tissue material
obstructing sinus drainage pathways and filling the sinuses, and air fluid
levels in acute sinusitis. Glaucoma, retrobulbar neuritis, hydrocephalus, and
infection also may cause aute headaches, evaluated with CT in clinically
doubtful cases.
B. Subacute headaches. Subacute headaches, particularly in the elderly, may be due to
a subdural hematoma, which canbleed more than once. CT is usually adequate for
both the initial evaluation and the follow-up, showing subdural space crescentic
collections. Acute blood is hyperdens, whereas chronic collections are hypodens

(FIG. 32.3).. CT is also adequate to diagnose hydrocephalus as dilated ventricular

cavities ( the temporal horns and the third ventricle are early reliable indicators of
hydrocephalus). Cerebral tumors and infections may be evaluated with postcontrast
CT (although contrast-enhanced MRI is superior), showing as enhancing masses,
possibly in a ring- enhancing pattern, with a chronic CSF leak, is a common reasin
for headaches causing recurrent ER visits, postcontrast MRI (particularly in the
coronal plane is diagnostic, showing thickened and densely enhancing meninges.
c. Chronic headaches. Unruptured AVMs, temporal arteritis, vasculitides,
intrascranial colloid cysts ogf the third ventricle, and cervical spondylosis are all
possible causes of chronic headaches, in addition to migraine, cluster headaches, and
chronic sinusitis. MRI currently has the best yield in screening patients with a
suspected intracranial anomaly.
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II.

SEIZURES
A. New onset adult seizures. MRI is currently and by far the preffered
initial maging metod to investigate new onset adult seizures, owing to
its superior contrast resolution and multiplanar capability. Magnetoencephalography (MEG) is a new technique that measures magnetic
fields due to neuronal activity, with a spatial resolutions of a few
millimeters and a temporal resolution of miliseconds; as of 2007, 30
MEG systems are installed in the Unitade States, 70% in intitutions
with a level 4 epilepsy program. MRI uses MEG in combination with
MRI in the same machine, and has currently the highest yield to detect
epiloptogenicfoci. Spect and PET imaging have extremely high
specifity if obtained duraing and ictus, but have limited use in clinical
practice. New onset adult seizures may be caused by brain tumors
(primary or metastatic), AVMs, inflammatory conditions, vasculitides,
ischemic lesions, gliotic scars from prior injury (both penetrating and
mild), again all conditions in which MRI has significant priority over
CT.
In patients with temporal lobe epilepsy, coronal MRI (FLAIR
and T2) has a high overall detection rate (up to 80%) for
hippocampal sclerosis (FIG. 32.4), showing an atrophic
hippocamous with high t2 signal, and indirect signs like a
dilated choroidal fissure and forniceal atrophy. Anterior

temporal lobectomy is recommended and may be curative in

cortical dysplasias. Presurgical evaluation includes evaluation
of hemispheric language dominance, usually obtained by
WADA testing )selective internal carotid artery injection of
sodium amobarbital). Functional MRI has been used to detect
language dominance, although its accuracy currently remains
questionable compared to the WADA test
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B. pediatric seizures. Infants with germinal matrix and traumatic hemorrhages,
intracranial neonatal infextions, and perinatal ischemia may be adequately evaluated
and followed with CT. in stable infants, most neonatal seizures are related congenital
disorders( migrational anomalies and structural defects), which are best evaluated
with MRI, although dramataic lesions are detectable on CT . in childhood- onset
seizures, clinical and EEG evaluations are usually adequate and imaging is not
indicated for certain forms of epilepsy, like febrile, absence (petit mal) seizures,
infantile spasm (lennox-Gastaut syndrome), anf benign focal epilepsy, unless the
child has abnormal physical findings or delayed development. Certain froms of
childhood epilepsy, like juvenile myoclonic epilepsy, are associated with a higher
frequency of structural anomalies requiring MRI evaluation.
III.

DEMENTIA
Cognitive decline may be related to
1)
2)
3)
4)

Depression
Structural lesion (cerebral tumor, subdural hematoma, hydrocephalus)
Chronic cerebral ischemia
Primary dementing onditions, the most common of which Alzheimer/s
disease (AD). A thorough clinical evaluation plays a major role in
these patients who are often in the older are group. Neuroimaging
detects correctable causes of dementia, found in about 5% of patients
with progressive cognitive decline. CT is adequate is conditions like
severe hydrocephalus and chronic subdural hematomas. However,
MRI is overall superior CT in the vast majority of patients, although
unfortunately corrective theraphy is only available in few conditions .
for example assessment of generalized cerebral and focal hippocampal
atrophy in AD is more easily done with MRI, including computerized

volumetric measurement of the hippocampus, considered promising

(although atrophy that is detectable and measurable is considered
beyond preventive theraphy). PET an SPECT presumably allow
detection of AD earlier by showing decreased hippocampal glucose
metabolism. Also MRS may show increased mayo-inositol and
decreased N-acetyl-aspartate (NAA) peaks in the gray matter. Vascular
dementia is also well evaluated by MRI, particularly FLAIR imaging,
which demonstrates lacunar infarcts and white matter abnormalities.
These lesions may have a typical distributin( periventricular, anterior
temporal, and subinsular) in certain conditions, that is cerebral
autosomal dominant arteriopathy with subcortical infarcts and
leukoencephalopathy (CADASIL). In picks disease and other
frontotemporal dementias, predominance of frontal lobe atrophy is
well evaluated on multiplanar MRI. In suspected normal pressure
hydrocephalus (NPH), transependymal CSF flow may be present,
shown as periventricular bright T2 signal. The pattern and velocity of
CSF flow may be evaluated at the foramen magnum using phase
contrast flow techniques.
IV.

ALTERED LEVEL OF CONCIOUSNESS

Evaluation of a patient with an altered of consciousness (LOC) is perhaps the
most common reason for neurological consultation requiring immediate input
from neuroimaging, and a most challenging one, because often no history is
obtainable in these patients whose LOC varies between mild disorientation
and deep coma. Causes of altered LOC disorders, toxic substances ingestion
(suicide) attemps or accidental), and cerebral tumors (primary or metastatic).
The immediate concern in these patients is to rule out a major
indication for acute lifesaving intervention, like intracranial hemorrhage,
large acute infarctions. Impending tonsillar or transtentorial herniation, or
other lie threatening conditions. CT scanning is the preffered neuroimaging
test in these patients because is easy to obtain and has great accuracy in
intracranial hemorrhage (intracerebral, SAH,SDH, epidural) and in assessing
in the risk for herniation if a lumbar puncture should be needed when a severe
meningeal infection is suspected. In patients without CT evidence of acute
abnormal findings, MRI should be obtained as soon as possible because some
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conditions not readily detectable by CT and requiring prompt therapy may be
clerarly seen at MRI. Examples include dural sinus thrombosis, which is well

V.

evaluated with cintrast-enhanced MRI and MR venography (MRV), acute

basilar artery thrombosis, diagnosed with DWI MRI, axial MRI and MR
angiography (MRA), hypertensive encephalopathy, and posterior reversible
encephalopathy syndrome )PRES), which show characteristic T2 and FLAIR
subcortical lesions, diffuse in hypertensive encephalopathy, predominantly
occipital in PRES.
CEREBRAL ISCHEMIA
Arterial supply to the brain may be acutely interrupted (acute stroke) or
chronically decreased with intermittent, usually progressively worsening
symptoms. Thorough clinical evaluation usually allows one to localize the
involved part of the brain. Venous ischemia results from occlusion of major
venous drainage channels, which can cause severe deficits culminating in
coma in diencephalic involvement from internal cerebral vein thrombosis.
A. Acute stroke. Acute stroke is an extreme emergency (time is brain).
There is a 3 hour window within stroke onset or the delivery of
intravenous tissue plasminogen activator (t-PA), the only currently
FDA-approved therapy for hyperacute management of ischemic
stroke. Past that, and up to 6 hours in the carotid circulation (possibly
longer in the vertebrobasilar circulation), intraarteial thrombolysis may
be offered in specialixed centers. An acceptable algorithm for the
emergency evaluation of acute stroke, currently technically attainable
in any medical institution, is to first obtain a plain CT, followed (if no
hemorrhage) by a contrast CTA and CT perfusion study to elevaluate
the perusion deficit (FIG.32.5). this is not only diagnostic , but also
prognostic as to the territory at risk, allowing to adjust hemodynamic
management. In some specialized centers, MRI,MRA (fig.32.6), and
MR perfusion are the standard protocol in acute stroke patients.
Diffusion weighted imaging (DWI) is positive for acute strokes as
early as 30 minutes and up to 10 day of the onset, and is therefore
particularly well suited to differentiate acute and subacute from
chronic events. Mismatch (size difference) between DWI and
perfusion deficits (especially a comparatively small DWI deficit)
requires special attention, prompting immediate thrombolysis (if
feasible) and hemodynamic support.
B. Dural sinus and cortical vein thrombosis. The venous intracranial
circulation should always be thoroughly evaluated, particularly if the
patients neurological deficit is accompanied by headache. Recent
thrombus within a dural sinus may be difficult to identify on plain CT

(although possibly seen as a spontaneously hyperdense filling

structures) or plain MRI ( hyperacute blood may apperar gray on both
T1 and T2 sequences). Therefore postcontrast imaging (CT and MRI)
has higner accuracy, showing clots as filling defects within a dural
sinus a cortical vein.MR venography (MRV) provides 3-D
visualization of the venous system, which may be selectively imaged
owing to its lower velocity profile compared to arterial structures.
C. Intermittent and chronic deficits. TIAs and chronic ischemic deficits
are best evaluated with MRI/MRA. DWI MRI is normal in TIAs and
ischemic lesions 10 days 4
D. Intermittent and chronic deficits. TIAs and chronic ischemic deficits
are best evaluated with MRI/MRA. DWI MRI is normal in TIAs and
ischemic lesions 10 days or older. MRI is far superior to CT to study a
number of stroke mimics like demyelinating disease and tumors. MRA
is very good for screening the intracranial and cervical arterial
vasculature (fig.32.6_), although yhe increasing resolution CTA (0,625
mm with current 64 detector scanners) provides excellent definition,
nearing that of conventional angiography
in certain location
(fig.32.7). severe arterial stenosis are known pitfallof MRA, which
exaggerates the degree of the lesion owing to signal loss.therefore,
conventional angiography remains indicated and useful in equivocal
cases whenever corrective therapy is considered ; endarterectomy or
stenting for carotid disease, or intracranial angioplasty or stenting for
intracranial stenosis.

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XII. MYELOPATHIES
Mri is the preffered imaging method in myelopathies, both aute and chronic,
providing direct mutiplanar imaging, superior cintrast between normal and abnormal
spinal cord, CSF, fat and bony structures. Gating techniques help reduce artifacts
from breathing and CSF, cardiac and vascular pulsations. Patients with acute
myelopathy and major contraindications to MRI (pacemakers) may be evaluated with
plain CT or CT myelography.
Nontraumatic acute myelopathy most often results from spinal cord
compression by a retripulsed neoplastic vertebral compression fractures, usually in an
elderly patient with an unknown (or known) cancer, best evaluated by noncintrast
whole spine MRI. Acute inflammatory myelopathy due to transverse myelitis or
demyelinating conditions is also best evaluated with MRI (Fig.32,8), with the
addition of contrast. Less commonly, acute myelopathy is due to spontaneous
epidural (or rare subdural ) hematomas. Traumatic cord contusions are best
evaluated by MRI using T2, STIR, and gradient echo sequences.
Causes of chronic myelopathy include spinal cord tumors. Degenerative
disease and disc herniations syringomyelia, congenital anomalies, that is,
diastematomyelia and tethere cord with or without associated lipomas, inflammatory
and demyelinating disease, and spinal dural arterovenous fistulae (Fig.32.9). initial
evaluation of these patients is also best undertaken with pre and postcontrast MRI.
CT myelography should be reserved for the rare patient with a major contraindication
MRI.